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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR Table of Contents   
Year : 2008  |  Volume : 19  |  Issue : 1  |  Page : 106-108
Fractional Excretion of Uric Acid as a Therapeutic Monitor in Cerebral Salt Wasting Syndrome

Department of Nephrology, Mediciti Hospitals, Hyderabad, Andhra Pradesh, India

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How to cite this article:
Soni SS, Adikey GK, Raman AS. Fractional Excretion of Uric Acid as a Therapeutic Monitor in Cerebral Salt Wasting Syndrome. Saudi J Kidney Dis Transpl 2008;19:106-8

How to cite this URL:
Soni SS, Adikey GK, Raman AS. Fractional Excretion of Uric Acid as a Therapeutic Monitor in Cerebral Salt Wasting Syndrome. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2021 Jun 24];19:106-8. Available from: https://www.sjkdt.org/text.asp?2008/19/1/106/37447
To the Editor:

Cerebral salt wasting syndrome (CSWS) is an underdiagnosed cause of hyponatremia that occurs in the setting of intracranial lesions. [1] Peters et al, first described it in 1950. The syndrome is characterized by excessive natriuresis leading to hyponatremic dehydra­tion in patients with intracranial disease. [2] This syndrome usually appears in the first week after brain injury and spontaneously resolves in two to four weeks. We describe a case of CSWS that occurred 6 weeks after cerebrovascular accident (CVA) (right temporoparietal infarction).

A 70-year- old man who was under reha­bilitation program following a CVA 6 weeks prior to admission in a stuperous condition. There was no history of convulsions or other localizing neurological features. On clinical examination, the patient was unconscious, looked dehydrated, but his vital signs were stable, and he had no new neurological deficits. The rest of the physical exam was unremarkable. The hematological investiga­tions and renal function tests were within normal limits. The electrolytes included sodium 104 mmol/L, potassium 4.2 mmol/L, chloride 78 mmol/L and serum uric acid 1.8 mg/dl. The thyroid and adrenal function tests were normal. Urinary spot sodium was 248 mmol/L in a urine volume of 4.2 liters in 24 hours. Fractional excretion of uric acid (FEUA) was 30%. Central venous pressure was 2 cm. Repeated CT scan and MRI scan did not reveal any new change in the CNS. Brain natriuretic peptide (BNP) levels were found to be elevated. A diagnosis of CSWS, as a delayed manifestation following stroke was made. Features suggestive of CSWS in our patient were hypovolemia, hyponatremia associated with polyuria, and high BNP and FEUA. The patient was treated with IV normal saline for 72 hours targeting correc­tion of electrolyte and volume. He was also started on fludrocortisone 0.1 mg/ day, which was continued for 4 weeks and tapered over 2 more weeks. Response to therapy was moni­tored with FEUA targeting a level <10%. The patient remained stable during and after discontinuation of mineralocorticoid therapy. His serum sodium and FEUA normalized later suggesting complete recovery.

CSWS is an often-unrecognized cause of hyponatremia in intracranial disorders. Common causes of CSWS include head injury, brain tumor, intracranial surgery, CVA, intracerebral hemorrhage and tuberculous meningitis. [3] Increased natriuretic peptides [4] and increased renal perfusion resulting in salt wasting are proposed mechanisms for this disorder. Differentiation of CSWS from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), another common cause of hyponatremia in this setting [5] [Table - 1], is crucial for appropriate therapy. CSWS usually requires fluid replacement and mineralocorticoid supplementation, while SIADH is treated with fluid restriction. Maesaka et al, have proposed utility of FEUA in CSWS with values >30% favoring the diagnosis. [6] We have successfully managed this case monitoring the level of FEUA.

   References Top

1.Yamanoto N, Miyamoto N, Seo H, Matui N, Kuwayama A, Terashima K. Hyponatremia with high plasma aterial natriuretic peptide levels. Report of two cases with emphasis on the pathophysiology of Central Salt Wasting. No Shinkei Geka 1987;15:1019-23.  Back to cited text no. 1    
2.Peters JP, Welt LG, Sims EA, Oriff J, Needham J. A salt wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians 1950;63:57-64.  Back to cited text no. 2    
3.Betjes MG. Hyponatremia in acute brain disease: The cerebral salt wasting syndrome. Eur J Intern Med 2002;13:9-14.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Barendes E, Walter M, Cullen P. Secretion of brain natriuretic peptide in patients with aneurismal subarachnoid hemorrhage. Lancet 1981;349:245.  Back to cited text no. 4    
5.Singh SK, Unnikrishnan AG, Reddy VS, Sahay RK, Bhadada SK, Agrawal JK. Cerebral salt wasting syndrome in a patient with a pituitary adenoma. Neurol India 2003;51:110-1.  Back to cited text no. 5    
6.Maesaka JK, Gupta S, Fishbane S. Cerebral salt-wasting syndrome: Does it exist? Nephron 1999;82:100-9.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]

Correspondence Address:
Sachin S Soni
Department of Nephrology, Mediciti Hospitals, Hyderabad, Andhra Pradesh
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PMID: 18087137

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